Key result
Traditional Chinese medicine may ameliorate myocardial fibrosis through mechanisms such as reducing inflammatory reaction and oxidative stress, inhibiting cardiac fibroblast activation, and regulating the TGF-β1/Smad signaling pathway.
Why the study?
Effective drugs for the treatment of myocardial fibrosis are lacking.
Does Traditional Chinese Medicine ameliorate myocardial fibrosis in preclinical models?
Does Traditional Chinese Medicine ameliorate myocardial fibrosis in preclinical models?
Traditional Chinese medicine offers potential candidate drugs for the prevention and treatment of myocardial fibrosis through multi-target regulatory mechanisms.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for TCM in myocardial fibrosis; leaves open clinical translation pending rigorous trials.
Effective drugs for the treatment of myocardial fibrosis (MF) are lacking. Traditional Chinese medicine (TCM) has garnered increasing attention in recent years for the prevention and treatment of myocardial fibrosis. This Article describes the pathogenesis of myocardial fibrosis from the modern medicine, along with the research progress. Reports suggest that Chinese medicine may play a role in ameliorating myocardial fibrosis through different regulatory mechanisms such as reduction of inflammatory reaction and oxidative stress, inhibition of cardiac fibroblast activation, reduction in extracellular matrix, renin-angiotensin-aldosterone system regulation, transforming growth Factor-β1 (TGF-β1) expression downregulation, TGF-β1/Smad signalling pathway regulation, and microRNA expression regulation. Therefore, traditional Chinese medicine serves as a valuable source of candidate drugs for exploration of the mechanism of occurrence and development, along with clinical prevention and treatment of MF.
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Ren et al. (2022) conducted a review in Myocardial fibrosis. Traditional Chinese Medicine was evaluated. Traditional Chinese medicine may ameliorate myocardial fibrosis through mechanisms such as reducing inflammatory reaction and oxidative stress, inhibiting cardiac fibroblast activation, and regulating the TGF-β1/Smad signaling pathway.
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